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P Bélanger

Publications and source records attributed to P Bélanger.

14 recordsLinked to original sources
PubMed2001

Effects of acute exercise on the gluconeogenic capacity of periportal and perivenous hepatocytes.

The present study was conducted to examine the effect of a single bout of exercise (rodent treadmill, 60 min at 26 m/min, 0% grade) on the gluconeogenic activity of periportal hepatocytes (PP-H) and perivenous hepatocytes (PV-H) in fasted (18 h) rats. Isolated PP-H and PV-H, obtained by selective destruction following liver perfusion with digitonin and collagenase, were incubated with saturating concentrations of alanine (Ala; 20 mM) or a mixture of lactate and pyruvate (Lac+Pyr; 20:2 mM) to determine the glucose production flux (J(glucose)) in the incubation medium. Results show that, in the resting conditions, J(glucose) from all exogenous substrates was significantly higher (P < 0.01) in PP-H than in PV-H. Exercise, compared with rest, resulted in a higher J(glucose) (P < 0.01) from Lac+Pyr substrate in the PV-H but not in the PP-H, resulting in the disappearance of the difference in J(glucose) between PP-H and PV-H. Exercise, compared with rest, led to a higher J(glucose) (P < 0.01) from Ala substrate in both PP-H and PV-H. However, the exercise-induced increase in J(glucose) (gluconeogenic activity) from Ala substrate was higher in PV-H than in PP-H, resulting, as from Lac+Pyr substrate, in the disappearance (P > 0.05) of the difference of J(glucose) between PP-H and PV-H. It is concluded that exercise differentially stimulates the gluconeogenic activity of PV-H to a larger extent than PP-H, indicative of a heterogeneous metabolic response of hepatocytes to exercise.

Alanine↗
PubMed2000

Effects of supranormal liver glycogen content on hyperglucagonemia-induced liver glycogen breakdown.

The purpose of the present study was to test the hypothesis that a higher hepatic glycogen level is associated with higher glucagon-induced hepatic glycogen depletion. Four groups of anesthetized rats received three injections (at times 0, 30, and 60 min) of glucagon (intravenously, 20 [microg/kg). Among these groups, hepatic glycogen levels had previously been manipulated either by an overloading diet (Fast-refed), a reduction in food intake (1/2-fast), or exercise (75 min of running, 26 m/ min, 0% grade). A fourth group had normal hepatic glycogen levels. A fifth group of rats was injected only with saline (0.9% NaCl). Liver glycogen concentrations were measured every 30 min during the course of the 90-min experiment, using liver samples obtained from the open liver biopsy technique. Plasma glucagon concentrations were significantly higher (P < 0.05) in the glucagon-injected groups than in the saline-injected group. As expected, liver glycogen levels were significantly higher (P < 0.01; 1.6-fold) in the Fast-refed group than in all other groups. Glucagon-induced decreases in liver glycogen concentrations were similar in Fast-refed than in normally fed and exercised rats when the overall 90-min period was considered. However, during the course of the last 30-min period, liver glycogen was significantly (P < 0.01) decreased only in the Fast-refed group. The Fast-refed, normally fed, and exercised groups had a similar glucagon-induced hyperglycemia that was significantly more elevated (P < 0.01) than glucose levels measured in the saline-injected group. Glucagon-induced reactive hyperinsulinemia was observed only in the Fast-refed and normally fed rats, and not in the exercised and 1/2-fast rats. It is concluded that supranormal levels of liver glycogen may be associated with a larger hyperglucagonemia-induced liver glycogen breakdown.

Animal Nutritional Physiological Phenomena↗
PubMed2000

Evidence that a decrease in liver glycogen content stimulates FFA mobilization during exercise.

This study evaluated a liver glycogen content decrease before exercise on the metabolic responses during exercise. Rats injected with glucagon (20 microg x kg(-1)) were compared to rats with a 50% food restriction (1/2-fast) and normally fed rats. All were studied at rest and during exercise (26 m/min, 0% grade). Resting liver glycogen concentrations were twice as high (P<.01) in normally fed rats, with no significant differences between 1/2-fast and glucagon-injected rats. During exercise, liver glycogen content was significantly reduced in normally fed rats. After exercise, plasma insulin levels were decreased (P<.01) in all groups, and beta-hydroxybutyrate concentrations were similar in normally fed and glucagon-injected rats and significantly (P<.01) lower in 1/2-fast rats. Exercise caused a significant increase in FFA concentrations in all groups (P<.01). No significant differences in FFA concentrations were found between 1/2-fast and glucagon-injected groups (P>0.05).

Analysis of Variance↗
PubMed1987

Metabolic synthesis of arylacetic acid antiinflammatory drugs from arylhexenoic acids. 2. Indomethacin.

Arylacetic acid antiinflammatory drugs can be metabolically produced by beta-oxidation of a 6-arylhex-5-enoic acid side chain. Such a mechanism provides for an in vivo sustained release of the active principle indomethacin from 6-[N-(p-chlorobenzoyl)-2-methylindol-3-yl]hex-5-enoic acid (7). Similarly, biphenylacetic acid was produced from both 6-(4'-biphenylyl)hex-5-enoic acid and its lower even homologue, 4-(4'-biphenylyl)but-3-enoic acid. The indole derivative produced sustained analgesia in a yeast-induced hyperalgesia model over a 12-h period. Indomethacin plasma levels of 2 micrograms/mL were observed for up to 24 h. Such levels were less than those achieved for the analogous case in which biphenylacetic acid was produced from biphenylylhex-5-enoic acid, suggesting metabolic discrimination between hex-5-enoic substrates. When indomethacin was dosed in equipotent analgesic levels, the level of circulating drug was considerably higher than that seen for metabolically derived drug. Hence 6-hex-5-enoic acid derivatives of indomethacin are metabolized to indomethacin in vivo to give sustained analgesia at low apparent circulating plasma levels of free drug. The possibility of tissue compartmentalization enhancing biological efficacy is suggested by these observations.

Animals↗
PubMed1987

L-641,953 (R-8-fluoro-dibenzo[b, f]thiepin-3-carboxylic acid-5-oxide): a novel thromboxane-prostaglandin endoperoxide antagonist.

The effects of L-641,953 (R-8-fluoro-dibenzo[b, f]thiepin-3-carboxylic acid-5-oxide) have been studied on pulmonary and other smooth muscle preparations in vitro and in vivo. When studied in vitro on guinea-pig tracheal chains, L-641,933 produced significant shifts in the dose-response curves to the prostaglandin endoperoxide analogues, U-44069 (pA2 7.06) and U-46619 (pA2 7.14), and prostaglandin (PG) F2 alpha (pA2 6.33) had minimal activity against contractions induced by histamine (pA2 4.38), 5-hydroxytryptamine (pA2 4.63), and acetylcholine (pA2 4.56) and slightly enhanced relaxation induced by PGE2. When tested on the guinea-pig gall bladder strip in vitro, L-641,953 antagonized contractions induced by U-44069 (pA2 7.03) but was less active against those induced by PGF2 alpha (pA2 6.03), PGE1 (pA2 5.62), and histamine (pA2 4.84). When tested in vitro on the guinea-pig pulmonary artery, L-651-953 significantly antagonized contractions induced by U-44069 (pA2 7.04), U-46619 (pA2 7.14), and PGF2 alpha (pA2 7.16) but was less effective against contractions induced by histamine (pA2 4.19). Schild analysis indicated that L-641,953 was fully competitive against contractions of either the guinea-pig tracheal chain induced by U-46619 or the guinea-pig pulmonary artery induced by U-44069 and U-46619. When tested on human platelets in vitro L-641,953 inhibited aggregation induced by U-44069 (IC50 1.3 X 10(-6) M) but not ADP.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1983

Synthesis and receptor binding studies relevant to the neuroleptic activities of some 1-methyl-4-piperidylidene-9-substituted-pyrrolo[2,1-b][3]benzazepine derivatives.

The synthesis of a series of 1-methyl-4-(9-substituted-11H-pyrrolo[2,1-b]benzazepin-11-ylidene)piperidines (4a-f) and 1-methyl-4-(9-substituted-6,11-dihydro-5H-pyrrolo[2,1-b][3]benzazepin-11-ylidene)piperidines (4g-l) is described. As with th e 3-substituted cyproheptadine compounds 1b-e, atropisomerism exists in 4b-f, but unlike the enantiomers of 1b-e, the pyrrolobenzazepine enantiomers racemize at room temperature. Thus, the bromo compound (+)-4b has a half-life of 128 +/- 1 min at 25 degrees C, while the chloro compound (-)-4c has a half-life of 114 +/- 9 min at 25 degrees C. Compounds 4a-l have been examined for receptor binding affinities in assays that have been recognized as predictive for antipsychotic activity. The displacement of specifically bound tritiated ligands, comprising the dopamine antagonist [3H]spiperone, the dopamine agonist [3H]apomorphine, the muscarinic cholinergic antagonist [3H]quinuclidinyl benzilate (QNB), the alpha-adrenergic antagonist [3H]prazosin, the alpha-adrenergic agonist [3H]clonidine, the serotonin-1 binding agent [3H]serotonin, and the mixed serotonin agonist-antagonist [3H]lysergic acid diethylamide (LSD), by 4a-l has been measured utilizing membrane preparations of mammalian brain. Certain of the features of the receptor binding of these compounds have been shown to be common to several of the receptor sites. Data from these binding studies have been compared to corresponding data previously obtained for a series of chiral 3-substituted cyproheptadine analogues, and the receptor binding data of the two classes of compounds are discussed with respect to their molecular geometries.

Animals↗
PubMed1975

Characteristics of in vitro ammonia and glucose production by dog kidney cortex.

Renal cortex slices from acidotic dogs incubated with L-glutamine 1 mM at pH 7.05 produced more ammonia and glucose than slices from nonacidotic animals but no significant difference could be demonstrated at pH 7.48. At a phosphate concentration of 20-30 mM in the medium, a 20-30% increase in ammonia and a 25-40% decrease in glucose production were observed. At L-glutamine concentrations from 0 to 8 mM, a curvilinear increase in both ammonia and glucose production was noted, the effect being greater in slices from acidotic animals. D-Glutamine had little effect on ammoniagenesis. Ammonia production (1 mM L-glutamine) in vitro was 50% lower in acidotic dogs than in vivo. Slices from the remnant left kidney (4-6 wk after right nephrectomy) did not behave differently during acidosis than those from the right kidney with regard to ammonia or glucose production. In vitro ammonia and glucose production was higher in the rat than in the dog in acidotic and nonacidotic conditions when comparable concentrations of L-glutamine substrate were used.

Ammonia↗